Alzheimer's disease: a challenging enigma.
The gray matter of patients dying of senile dementia of the Alzheimer type (SDAT) displays severe histopathologic lesions, including neurofibrillary tangles, neuritic (senile) plaques, granulovacuolar degeneration, Hirano bodies, and loss of nerve cells. The differences between the changes seen in SDAT and those seen in normal aging of the brain are quantitative. Results of neurochemical studies suggest that cholinergic neurons are especially afflicted, but clinical trials administering choline precursors in patients' food hve thus far been unsuccessful. Theories of its cause include genetic predisposition, an exogenous toxin, and a slow (latent) viral agent. No fully satisfactory animal model exists for this disorder, so prospective clinicopathologic investigations using tissues harvested at the time of autopsy may help elucidate the pathogenesis of this, the most common form of organic dementia.
D000375:Aging; D000818:Animals; D001921:Brain / Q000378:metabolism / Q000473:pathology; D002540:Cerebral Cortex / Q000378:metabolism / Q000473:pathology; D002794:Choline / Q000378:metabolism; D002795:Choline O-Acetyltransferase / Q000378:metabolism; D002799:Cholinergic Fibers / Q000378:metabolism / Q000473:pathology; D003704:Dementia / Q000209:etiology* / Q000378:metabolism / Q000473:pathology*; D004285:Dogs; D000882:Haplorhini; D006801:Humans; D051379:Mice; D009454:Neurofibrils / Q000473:pathology / Q000648:ultrastructure; D051381:Rats; D014617:Vacuoles / Q000473:pathology
D002795:Choline O-Acetyltransferase; D002794:Choline